The cell cycle is controlled by extracellular signals such as growth factors and growth inhibitors and, internally, by a series of kinases known as the cyclin-dependent kinases or cdk's. Cell cycle progression is largely dependent on the orderly activity of these cdk's. The first cyclin-dependent kinase identified was the cdc28 gene of the yeast Saccharomyces cerevisiae. Conditional mutants of cdc28 lead to G1 arrest. In the same genetic screen that identified cdc28, another gene which gave the same phenotype was discovered and termed cdc37. Although much has been learned about cdc28 and cyclin-dependent kinases in the last ten years, relatively little is known about cdc37. In yeast, the phenotype of cdc37 results from a failure to activate the cdc28 kinase in those cells. This failure appears to be due to an inefficient association of cdc28 with cyclins in the yeast Saccharomyces cerevisiae. This observation has led to the hypothesis that cdc37 might function as an assembly factor for the cdc28 cyclin complex.
Aberrant activity associated with molecules involved in cell cycle control is responsible, in some instances, for oncogenic transformation. Additional information relating to the interaction of cdc37 with other important cellular signalling molecules may provide the basis for targeted therapeutic intervention.